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Review
. 2014 Jul 3;371(1):58-66.
doi: 10.1056/NEJMra1214243.

Acute kidney injury and chronic kidney disease as interconnected syndromes

Lakhmir S Chawla  1 , Paul W Eggers, Robert A Star, Paul L Kimmel
Affiliations
Review

Acute kidney injury and chronic kidney disease as interconnected syndromes

Lakhmir S Chawla et al. N Engl J Med. .
No abstract available

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Figures

Figure 1.
Figure 1.. Acute Kidney Injury and Chronic Kidney Disease as an Interconnected Syndrome.
Acute kidney injury and chronic kidney disease share common risk factors and disease modifiers. When acute kidney injury occurs without preexisting kidney disease, chronic kidney disease still may develop. Conversely, the presence of chronic kidney disease is an important risk factor for the development of acute kidney injury. Either acute kidney injury or chronic kidney disease (and presumably their combination) is associated with an increased risk of death and may result in complications such as cardiovascular disease, progressive decreases in kidney function, diminished quality of life, and the development and progression of disability. ESRD denotes end-stage renal disease.
Figure 2.
Figure 2.. Pathophysiological Features of Acute Kidney Injury Leading to Chronic Kidney Disease.
The architecture of normal kidney tissue is compared with that of injured tissue after an episode of acute kidney injury. Injured tissue shows alteration of tissue architecture and cell structure, including changes in the brush border. A variety of pathologic processes are initiated in injured and regenerating cells, including premature cell-cycle arrest, activation of myofibroblasts and fibrocytes, recruitment of various infiltrating immune and bone marrow cells to the site of injury, vascular dropout, and fibrosis. The change in tissue architecture leads to altered anatomical relationships between structures and a tissue microenvironment that promotes additional fibrosis and vascular dropout. Specific subpopulations of cells such as macrophages and T cells, differentially recruited into injured kidney tissues, may determine whether organ responses are ameliorative or maladaptive. The factors mediating recruitment, the populations of cells in human tissues that will have different responses leading to different long-term outcomes, and the interaction of recruited cells to determine outcomes are still incompletely understood. The inset shows renal tubular epithelial cells after an episode of acute kidney injury. Representative examples from various experimental studies in animals are listed in the inset. The fate of the cell, as well as the microenvironment and organ, depends on the balance between the results of repair and regenerative pathways, including apoptosis, dedifferentiation, and proinflammatory and antiinflammatory, epigenetic, and profibrotic changes. These processes may occur differentially in heterogeneous cell sets in the kidney microenvironment. Specific macrophage and T-cell subsets, as well as certain cytokines and immunoreactants, may be associated with either injury or repair. The chronic dysregulation of these factors over time and their net interactions are likely to determine the extent of fibrotic responses and organ function. BMP-7 denotes bone morphogenetic protein 7, TGF-β transforming growth factor β, and Tregs regulatory T cells.
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